| 1. |
- Chapman, C. L., et al.
(author)
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Occupational heat exposure and the risk of chronic kidney disease of nontraditional origin in the United States
- 2021
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In: American Journal of Physiology-Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 321:2
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Journal article (peer-reviewed)abstract
- Occupational heat exposure is linked to the development of kidney injury and disease in individuals who frequently perform physically demanding work in the heat. For instance, in Central America, an epidemic of chronic kidney disease of nontraditional origin (CKDnt) is occurring among manual laborers, whereas potentially related epidemics have emerged in India and Sri Lanka. There is growing concern that workers in the United States suffer with CKDnt, but reports are limited. One of the leading hypotheses is that repetitive kidney injury caused by physical work in the heat can progress to CKDnt. Whether heat stress is the primary causal agent or accelerates existing underlying pathology remains contested. However, the current evidence supports that heat stress induces tubular kidney injury, which is worsened by higher core temperatures, dehydration, longer work durations, muscle damaging exercise, and consumption of beverages containing high levels of fructose. The purpose of this narrative review is to identify occupations that may place US workers at greater risk of kidney injury and CKDnt. Specifically, we reviewed the scientific literature to characterize the demographics, environmental conditions, physiological strain (i.e., core temperature increase, dehydration, heart rate), and work durations in sectors typically experiencing occupational heat exposure, including farming, wildland firefighting, landscaping, and utilities. Overall, the surprisingly limited available evidence characterizing occupational heat exposure in US workers supports the need for future investigations to understand this risk of CKDnt.
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| 2. |
- Hansson, Erik, 1987, et al.
(author)
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Markers of kidney tubular and interstitial injury and function among sugarcane workers with cross-harvest serum creatinine elevation
- 2022
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In: Occupational and Environmental Medicine. - : BMJ. - 1470-7926 .- 1351-0711. ; 79:6, s. 396-402
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Journal article (peer-reviewed)abstract
- Objectives Serum creatinine (SCr) is a routine marker of kidney injury but also increases with dehydration and muscular work. This study was to elucidate whether increase in SCr is associated with more specific markers of kidney tubular and interstitial injury and function, during prolonged heat stress among workers at high risk of chronic kidney disease of non-traditional origin (CKDnt). Methods Urine monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), calbindin, glutathione S-transferase-pi (GST-pi), clusterin, interleukin 18 and albumin, fractional excretion of potassium (FEK), blood haemoglobin, serum potassium, ferritin and erythropoietin were measured before and after harvest in a sample of 30 workers with a >= 0.3 mg/dL SCr increase across harvest (cases), and 53 workers with stable SCr (controls). Results Urine MCP-1 (p for differential cross-harvest trend <0.001), KIM-1 (p=0.002), calbindin (p=0.02), GST-pi (p=0.04), albumin (p=0.001) and FEK (p<0.001) increased in cases, whereas blood haemoglobin (p<0.001) and serum erythropoietin (p<0.001) decreased. Conclusion Several markers of tubular and interstitial injury and function changed as SCr increased across a harvest season, supporting the use of SCr as an indicator of kidney injury in physically active workers regularly exposed to heat stress. Repeated injury similar to that described here, and continued work under strenuous and hot conditions with similarly elevated injury markers is likely to worsen and possibly initiate CKDnt.
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| 3. |
- Pearson, J., et al.
(author)
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Active and passive heat stress similarly compromise tolerance to a simulated hemorrhagic challenge
- 2014
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In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 307:7, s. R822-R827
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Journal article (peer-reviewed)abstract
- Passive heat stress increases core and skin temperatures and reduces tolerance to simulated hemorrhage (lower body negative pressure; LBNP). We tested whether exercise-induced heat stress reduces LBNP tolerance to a greater extent relative to passive heat stress, when skin and core temperatures are similar. Eight participants (6 males, 32 +/- 7 yr, 176 +/- 8 cm, 77.0 +/- 9.8 kg) underwent LBNP to presyncope on three separate and randomized occasions: 1) passive heat stress, 2) exercise in a hot environment (40 degrees C) where skin temperature was moderate (36 degrees C, active 36), and 3) exercise in a hot environment (40 degrees C) where skin temperature was matched relative to that achieved during passive heat stress (similar to 38 degrees C, active 38). LBNP tolerance was quantified using the cumulative stress index (CSI). Before LBNP, increases in core temperature from baseline were not different between trials (1.18 +/- 0.20 degrees C; P > 0.05). Also before LBNP, mean skin temperature was similar between passive heat stress (38.2 +/- 0.5 degrees C) and active 38 (38.2 +/- 0.8 degrees C; P = 0.90) trials, whereas it was reduced in the active 36 trial (36.6 +/- 0.5 degrees C; P <= 0.05 compared with passive heat stress and active 38). LBNP tolerance was not different between passive heat stress and active 38 trials (383 +/- 223 and 322 +/- 178 CSI, respectively; P = 0.12), but both were similarly reduced relative to active 36 (516 +/- 147 CSI, both P <= 0.05). LBNP tolerance is not different between heat stresses induced either passively or by exercise in a hot environment when skin temperatures are similarly elevated. However, LBNP tolerance is influenced by the magnitude of the elevation in skin temperature following exercise induced heat stress.
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